Aflatoxin mutagenesis and metabolism and their dietary modification in rainbow trout (Salmo gairdneri) Public Deposited

http://ir.library.oregonstate.edu/concern/graduate_thesis_or_dissertations/rx913s20f

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  • Aflatoxin B₁ (AFB₁) is a mold-produced toxin which has been shown to be a potent hepatocarcinogen in many animal species. Of the species studied thus far, rainbow trout have proven to be the most sensitive. Experiments were conducted to investigate various aspects of AFB₁ metabolism in this species, including in vitro mutagenesis, and effects of dietary modifiers of AFB, carcinogenesis on in vitro metabolism and mutagenesis. A comparative study of AFB₁ metabolism in two salmonid species was also conducted. In the first study, the relative mutagenic potencies of several alfatoxin metabolites were evaluated using a trout liver fraction system. Preliminary studies characterizing trout liver fractions for use as an activation system were described. The results from comparative mutagenicity experiments demonstrated that in vitro mutagenic potencies qualitatively correlated with the in vivo carcinogenic activities of various aflatoxins in rainbow trout. The importance of these findings is discussed. In the second study fish hepatocytes were characterized to examine possible differences in activation of AFB₁ to bacterial mutagens by hepatocytes from rainbow trout and coho salmon, two species which are known to differ markedly in sensitivity to the carcinogenic effects of AFB₁. Activation efficiency was approximately three times greater in hepatocytes from trout compared to salmon. A more marked difference was seen when S20 liver fractions from the two species were used. Analysis of unbound [³H]AFB₁ metabolites revealed that trout hepatocytes metabolized [³H]AFB₁ to a greater extent than salmon. The results accurately reflected in vivo carcinogenesis trends in salmonid fish. Additional experiments were conducted to evaluate the effects of dietary modifiers of AFB₁ carcinogenesis on in vitro mutagenesis and metabolism of AFB₁. Dietary β-naphthoflavone (β-NF) was shown to induce the production of a novel trout metabolite of AFB₁, aflatoxicol M₁ (AFL-M₁). AFL-M₁ exhibited a mutagenic potency less than AFB₁ or aflatoxicol (AFL), but greater than that of aflatoxin-M₁ (AFM₁). Dietary β-NF, however, appeared to have no effect on in vitro mutagenic activation of AFB₁ using hepatocytes or liver S20 fraction from trout. Dietary PCBs (Aroclor 1254) was shown to significantly decrease in vitro mutagenesis of AFB₁, which reflected a similar PCB-mediated inhibitory effect on AFB₁ carcinogenesis in trout in vivo. Cyclopropenoid fatty acids (CPFAs) present in the diet (0-600 ppm) were shown to have no effect on in vitro mutagenesis of AFB₁, indicating CPFAs may not significantly alter in vivo initiation of AFB₁ carcinogenesis.
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